Underground azelaic acid–conferred resistance to pseudomonas syringae in arabidopsis

Nicolás M. Cecchini, Suruchi Roychoudhry, De Quantarius J. Speed, Kevin Steffes, Arjun Tambe, Kristin Zodrow, Katerina Konstantinoff, Ho Won Jung, Nancy L. Engle, Timothy J. Tschaplinski, Jean T. Greenberg

Research output: Contribution to journalArticlepeer-review

35 Scopus citations

Abstract

Local interactions between individual plant organs and diverse microorganisms can lead to whole plant immunity via the mobilization of defense signals. One such signal is the plastid lipid-derived oxylipin azelaic acid (AZA). Arabidopsis lacking AZI1 or EARLI1, related lipid transfer family proteins, exhibit reduced AZA transport among leaves and cannot mount systemic immunity. AZA has been detected in roots as well as leaves. Therefore, the present study addresses the effects on plants of AZA application to roots. AZA but not the structurally related suberic acid inhibits root growth when directly in contact with roots. Treatment of roots with AZA also induces resistance to Pseudomonas syringae in aerial tissues. These effects of AZA on root growth and disease resistance depend, at least partially, on AZI1 and EARLI1. AZI1 in roots localizes to plastids, similar to its known location in leaves. Interestingly, kinases previously shown to modify AZI1 in vitro, MPK3 and MPK6, are also needed for AZA-induced root-growth inhibition and aboveground immunity. Finally, deuterium-labeled AZA applied to the roots does not move to aerial tissues. Thus, AZA application to roots triggers systemic immunity through an AZI1/EARLI1/MPK3/MPK6-dependent pathway and AZA effects may involve one or more additional mobile signals.

Original languageEnglish
Pages (from-to)86-94
Number of pages9
JournalMolecular Plant-Microbe Interactions
Volume32
Issue number1
DOIs
StatePublished - 2019

Funding

†Corresponding author: Jean T. Greenberg; E-mail: [email protected] Funding: This research was supported by a National Science Foundation grant IOS1456904 to J. T. Greenberg. This research was also supported, in part, by the Genomic Science Program (Science Focus Area ‘Plant-Microbe Interfaces’), United States Department of Energy, Office of Science, Biological and Environmental Research to Oak Ridge National Laboratory, which is managed by UT-Battelle, LLC, for the United States Department of Energy under contract number DE-AC05-00OR22725. D. J. Speed was supported by National Institute of General Medical Sciences grant T32 GM007183 and a predoctoral fellowship award from the Ford Foundation. N. M. Cecchini is a career investigator of CONICET (Argentina). This research was supported by a National Science Foundation grant IOS1456904 to J. T. Greenberg. This research was also supported, in part, by the Genomic Science Program (Science Focus Area ‘Plant-Microbe Interfaces’), United States Department of Energy, Office of Science, Biological and Environmental Research to Oak Ridge National Laboratory, which is managed by UT-Battelle, LLC, for the United States Department of Energy under contract number DE-AC05-00OR22725. D. J. Speed was supported by National Institute of General Medical Sciences grant T32 GM007183 and a predoctoral fellowship award from the Ford Foundation. N. M. Cecchini is a career investigator of CONICET (Argentina). We thank S. C. Jiang and J. Jelenska for helpful discussions. We thank C. Castresana for the kind gift of synthetic ONA.

FundersFunder number
United States Department of EnergyDE-AC05-00OR22725
National Science FoundationIOS1456904
Ford Foundation
National Institute of General Medical SciencesT32GM007183
National Science Foundation

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